Todd Paresis

Article Author:
James Mastriana
Article Author (Archived):
Jeffrey Pay
Article Editor:
Roger Taylor
2/3/2020 1:20:18 PM
PubMed Link:
Todd Paresis


Todd Paresis is a syndrome associated with weakness or paralysis of part or all of the body after a focal-onset seizure. It most commonly affects one limb or one half of the body but can have a wide range of presentations. 

This condition was originally described by Irish physiologist Robert Bentley Todd in 1849 but has been further defined, researched, and explained by many others over the years. Despite this being a common phenomenon for neurologists, relatively little research has been conducted on the condition.


The current and most accepted understanding of the condition is theorized to be exhaustion of the primary motor cortex (or any other area of the brain) after neuronal hyperexcitation in a focal or diffuse seizure state.


Approximately 13% of all seizures show signs of Todd paresis in one presentation or another.[1] The syndrome does not appear to show a propensity for male, female, or any specific age or race.

A retrospective study on the condition found that postictal paralysis was observed most commonly (78% of patients studied) when patients displayed "obvious" clonic motor movement during the seizure activity. This is compared to only 10% of patients with no ictal motor activity.[1] The same study showed that unilateral clonic activity was the most common predictor of postictal paralysis in 56% of patients. Despite its relatively small sample size of 328, this study has value due to the lack of studies explaining the duration, seizure characteristics, and frequency of Todd paresis; however, it is likely based on the fact that only patients with medically intractable seizures were studied, making the study less likely to accurately apply to the general epileptic community.


The pathophysiology is most commonly theorized to be the result of one of three mechanisms. The first theory is that the area in question is depolarized so vigorously during the seizure that it enters a prolonged refractory period, making attempts at excitation require significantly higher voltage for depolarization. The second is that there is prolonged local inhibition by surrounding structures theorized to be a protective measure employed by the brain to prevent further seizure activity. The third explains this phenomenon by theorizing that blood flow to the affected area of the brain is restricted for a time through vasoconstriction thus limiting the function of that area through relative oxygen starvation. None of these theories has been definitively validated or even well studied at the time of this publication. 

With regards to the third theory, a study in 2017 using rodent models found that, during the postictal period,  significant decreases in pO2 (pO2 < 10mmHg) were found in localized areas of the brain leading to "memory and behavioral impairments." They also found an association between L-type calcium channels and cyclooxygenase activity as potential causative mechanisms behind the hypoperfusion. Rodents treated with and without postictal nifedipine treatment were studied. The researches found that untreated animals did indeed have a weakness in grip strength when compared to the nifedipine group. It is also of interest that 8 of 10 human models showed evidence of focal tissue hypoperfusion. Despite all of this exciting information on the potential mechanisms behind this condition, all the data must be interpreted with caution given that this a preliminary study and not well powered.[2]


The histopathologic changes associated with and the origin of this condition is not well understood and only minimally studied at this time.

History and Physical

The classic presentation of this condition is weakness observed in one limb contralateral to the seizure activity after a focal seizure has occurred. This can range from a mild weakness of the limb to complete paralysis; however, this syndrome is not limited to limb weakness and can include gaze palsy, aphasia, and sensory disturbances (e.g., neglect, anesthesia, visual field deficits) depending on the particular anatomic epileptic focus.[1][3][4]

It is important to understand that pure focal seizures may cause this condition, but it may also be observed in focal-onset seizures. The key difference being that a focal-onset seizure begins with twitching in one limb (or other effects depending on the initial focus), then to one complete half of the body, and then appearing as a more generalized seizure pattern (i.e., Jacksonian march). A pure focal seizure remains with the affected area of the body and does not become generalized.[3]

This postictal syndrome may last anywhere from minutes to days, with the vast majority of patients seeing spontaneous and complete resolution within 36 hours. Complete resolution of symptoms is seen within 15 hours on average.[3]

If the seizure was witnessed, it is important to ask the observer if any focal activity was observed prior. While this history can be very helpful, it is often too subtle for the witness to recall. This is especially true in a first seizure episode.


No laboratory studies help in making the diagnosis of postictal paralysis. 

CT perfusion scan anomalies are often noted but are not consistent and thus nondiagnostic. It can show a hyper- or hypoperfusion state at the site of epileptic focus.[5][6][5]

CT angiography is unremarkable in postictal paralysis. This can be used to differentiate between this condition and acute cerebrovascular accident.[7]

MRI will show findings consistent with a seizure such as a transiently increased T2 signal at the site of epileptic focus. This is due to increased edema (i.e., H2O molecules) at the site which is bright on T2 imaging. It is best appreciated on fluid-attenuated inversion recovery (FLAIR).[8]

Treatment / Management

Treatment of this condition is primarily supportive and typically resolves without any intervention. No randomized control trials are available to compare treatment modalities.

Differential Diagnosis

Cerebrovascular accident (embolic, hemorrhagic): This may be distinguished by hypoperfusion on CT angiography and MRI or evidence of intracranial hemorrhage on non-contrasted CT of the brain. 

Hemiplegic migraine: This is a rare genetic mutation or familial migraine variant in which the patient presents with severe, typically, unilateral headache and weakness, ataxia, or paralysis.[9]

Hemiconvulsion: Hemiplegia epilepsy syndrome: This clinical syndrome of infancy or early childhood (generally < 4 years old) is characterized by prolonged hemispheric seizure activity during a febrile disease, resulting in hemispheric atrophy and flaccid hemiplegia followed by focal seizures with an interval of months to years.[10]

Hypoglycemia: Hypoglycemia is a well-known mimic of stroke syndromes.


The prognosis of this condition is very good as the postictal paralytic symptoms are self-limited and require no intervention.


Typically, no complications are expected as the paresis is self limiting.


Neurology is typically consulted to evaluate Todd Paresis.

Enhancing Healthcare Team Outcomes

It is important to communicate findings of Todd Paresis with treating physicians.  Unilateral symptoms should always be addressed and discussed with treating physicians and nursing staff when they occur.  A careful history and physical exam can help exclude other causes of symptoms such as cerebrovascular accidents.  It is important that patients with seizure disorders be educated that this phenomenon can occur to prevent uneccessary over-testing. Patients who have experienced Todd's Paresis in the past should notify members of their care team.


[1] Gallmetzer P,Leutmezer F,Serles W,Assem-Hilger E,Spatt J,Baumgartner C, Postictal paresis in focal epilepsies--incidence, duration, and causes: a video-EEG monitoring study. Neurology. 2004 Jun 22     [PubMed PMID: 15210875]
[2] Lyman KA,Chetkovich D, New Insights Into Postictal Paresis: An Epilepsy-Associated Phenomenon That may not be as Benign as Long Thought. Epilepsy currents. 2017 May-Jun     [PubMed PMID: 28684952]
[3] Rolak LA,Rutecki P,Ashizawa T,Harati Y, Clinical features of Todd's post-epileptic paralysis. Journal of neurology, neurosurgery, and psychiatry. 1992 Jan     [PubMed PMID: 1548500]
[4] Fernandes PM,Whiteley WN,Hart SR,Al-Shahi Salman R, Strokes: mimics and chameleons. Practical neurology. 2013 Feb     [PubMed PMID: 23315456]
[5] Payabvash S,Oswood MC,Truwit CL,McKinney AM, Acute CT perfusion changes in seizure patients presenting to the emergency department with stroke-like symptoms: correlation with clinical and electroencephalography findings. Clinical radiology. 2015 Oct     [PubMed PMID: 26155937]
[6] Mathews MS,Smith WS,Wintermark M,Dillon WP,Binder DK, Local cortical hypoperfusion imaged with CT perfusion during postictal Todd's paresis. Neuroradiology. 2008 May     [PubMed PMID: 18278489]
[7] Gelfand JM,Wintermark M,Josephson SA, Cerebral perfusion-CT patterns following seizure. European journal of neurology. 2010 Apr     [PubMed PMID: 19968701]
[8] Binder DK, A history of Todd and his paralysis. Neurosurgery. 2004 Feb     [PubMed PMID: 14744294]
[9] Kumar A,Arora R, Headache, Migraine Hemiplegic null. 2018 Jan     [PubMed PMID: 30020674]
[10] Tenney JR,Schapiro MB, Child neurology: hemiconvulsion-hemiplegia-epilepsy syndrome. Neurology. 2012 Jul 3     [PubMed PMID: 22753451]